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March 1974

Experimental Carbon Monoxide Encephalopathy in the Primate: I. Physiologic and Metabolic Aspects

Author Affiliations

Bethesda, Md
From the Laboratory of Perinatal Physiology, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Public Health Service, Dept of Health, Education, and Welfare, Bethesda, Md. Dr. Ginsberg is now with the Department of Neurology, Hospital of the University of Pennsylvania, Philadelphia.

Arch Neurol. 1974;30(3):202-208. doi:10.1001/archneur.1974.00490330010002

Nineteen rhesus monkeys received single exposures to carbon monoxide (CO) sufficient to produce consistent neuropathologic lesions. Inhalation of 0.2% CO led to stable plateau levels of blood carboxyhemoglobin, which averaged 76%. The mean arterial blood oxygen content of these animals declined to 4.2 ml/100 ml. The arterial oxygen pressure remained normal. The jugular venous oxygen content exceeded that of the central venous blood during and following the intoxication. Arterial hypotension and metabolic acidosis evolved consistently though to a variable extent. The central venous pressure remained unaltered. Severe respiratory depression occurred only rarely, whereas cardiac arrhythmias constituted a major risk to life during the actual exposure. Ventricular fibrillation occurred in four animals and was fatal in two but could be largely prevented by the use of lidocaine prophylactically. Arterial hypotension led to the death of two animals.

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